REFERAT

“Management Anesthesia of Preeclampsia with CHF”

Neneng Miratunisa (H1A013043)

SUPERVISOR :
dr. Ni Made Ayu Suria Mariati, Sp.An
Introduction

 Preeclampsia, along with the other hypertensive disorders of pregnancy is a leading

cause of maternal morbidity and mortality.
 Preeclampsia affects the 5-8% of all pregnancies worldwide. Deaths are due to
intracranial haemorrhage, respiratory failure and hepatic failure or rupture.
 Severe maternal complications include antepartum haemorrhage due to placental
abruption, eclampsia, cerebrovascular accidents, organ failure and disseminated
intravascular coagulation.
 Pre-eclampsia is the leading cause of fetal growth restriction, intrauterine fetal demise and
preterm birth.
Con’t

 Preeclampsia is associated with reduction in intravascular volume, haemoconcentration

and hypoproteinenia. Pulmonary edema is significant cause of maternal and perinatal
morbidity and mortality in one large series.
 The incidence of pulmonary edema was also higher in older multigravida and in those
with chronic hypertension. Pulmonary edema complicates around 0.05% of low-risk
pregnancies but may develop in up to 2.9% of pregnancies complicated by
preeclampsia.
Definition

 Pre-eclampsia is generally defined as new hypertension (systolic blood pressure ≥140

mmHg diastolic blood pressure of ≥90 mm Hg) and substantial proteinuria (≥300 mg in 24
h) at or after 20 weeks of gestation.
 Preeclampsia remains one of the leading causes of global maternal and perinatal
morbidity and mortality, particularly in resource-restrained settings.
 Known major maternal risk factors for preeclampsia include previous preeclampsia, in
particular early-onset disease, young maternal age, primiparity, pre-existing medical
conditions such as antiphospholipid syndrome, systemic lupus erythematosis, pre-existing
hypertension or diabetes, and multiparity.
Con’t

 The International Society for the Study of Hypertension in Pregnancy have revised
diagnostic criteria for preeclampsia, with proteinuria no longer an essential requirement.
 After 20 weeks’ gestation, new onset hypertension associated with either proteinuria,
evidence of end-organ involvement (thrombocytopaenia, renal insufficiency, impaired
hepatic function, pulmonary oedema and cerebral or visual symptoms), or utero-
placental dysfunction  is sufficient to make a diagnosis.
 Once diagnosed, it is recognised that preeclampsia can rapidly progress from ‘mild’
disease to severe end-organ involvement.
Cardiovascular Physiology During Pregnancy

 The physiological demands of pregnancy are partly met through changes in

cardiovascular physiology, which has to accommodate the extra metabolic demands
presented by the foetus and other organ systems required to perform an augmented
physiological role.
 Hence, the increase in uterine size and activity together with the blood flow into the
choriodecidual space are a significant component of the extra cardiovascular work
during pregnancy accounting for 12 % of the total cardiac output in a term pregnancy.
 The kidneys and the skin, in particular, have augmented perfusion to disperse heat and
allow the retention of sodium and water during pregnancy.
Con’t

 The increased blood volume secondary to hyperaldosteronism allows an increase in

cardiac output mediated by increased stroke volume and heart rate; the cardiac output
rises in the first trimester peaking towards the end of the second trimester at between 3.5
and 6 litres per minute (which is 30–50 % higher than non-pregnant values).
 The increased cardiac output is discharged into a dilated peripheral systemic circulation
that shows a falling systemic vascular resistance from the first trimester onwards.
 The extent of the adaptation is such that the arteriovenous oxygen difference falls during
early pregnancy and rises towards pre-pregnancy levels by the end of the pregnancy.
Con’t

 Both left and right ventricles show evidence of increased mass, volume and enddiastolic
volume during pregnancy. These changes reflect the increase in cardiac output and
intravascular blood volume and reverse after delivery.
 Figure 1: Summary of Physiological Changes Occurring During Pregnancy
Aetiology and Pathophysiology of Heart Failure in
Pregnancy

 Cardiovascular disease complicating pregnancy may be considered in groups including

those attributable to increased vascular resistance, diseases of the aortic root, heart
disease itself due to either obstruction, ventricular failure or congenital abnormalities of the
heart and proximal vasculature.
 Three pregnancy-specific causes of heart failure are identifiable (pre-eclampsia,
peripartum cardiomyopathy and amniotic fluid embolism) together with all the non-
pregnancyrelated causes of heart failure that may become co-morbid diseases
complicating pregnancy.
Increased Vascular Resistance

Pre-eclampsia
 Pre-eclampsia commonly results in pulmonary oedema that, together with
cerebrovascular haemorrhage.
 Pregnancy and pre-eclampsia are usually associated with a hyperdynamic circulation
and enhanced left ventricular contractility.
 In the case of pre-eclampsia, increased systemic vascular resistance may increase the
filling pressures in the left atrium and, together with intravenous fluid administration, will
increase the likelihood of developing pulmonary oedema.
Con’t

 The direct cardiac contribution to the development of pulmonary oedema is usually due
to diastolic dysfunction.
 The left ventricle tolerates an intravenous fluid load poorly showing a rapid rise in left-sided
filling pressures without any similar observable changes in the right heart.
 Occasionally mildly impaired systolic function will be identified in severe pre-eclampsia,
although this is usually transitory.
Con’t

Hypertensive Cardiomyopathy
 Chronic hypertension complicating pregnancy in the absence of superimposed pre-
eclampsia is not clearly associated with adverse maternal outcome.
 Chronic hypertension prior to pregnancy is, however, increasing in frequency due to the
worldwide obesity epidemic and is prevalent in 3 % of all US pregnant women.
 Chronic hypertension leads to increased frequency of preeclampsia (17–25 % versus 3–5 %
in the general population), as well as placental abruption, foetal growth restriction and
preterm birth.
Con’t

Pulmonary Hypertension and Right Heart Failure

 The symptoms suggestive of pulmonary hypertension are those exertional dyspnoea with
everyday activities.
 Weakness and recurrent syncope are also common. These symptoms may be followed by
signs consistent with right heart failure (increased jugularis venous pressure [JVP], loud
second heart sound/P2, hepatomegaly and peripheral oedema with clear lung fields).
Pathophysiology

 Although it is a well-studied disease, the pathophysiology of pre-eclampsia remains

uncertain. Several key features are thought to have a role in the development of pre-
eclampsia, which is mainly considered as a vascular disorder.
 The most probable causes for this disease are a failure of trophoblast invasion leading to a
failed transformation of the uterine spiral arteries, and an incorrect deep placentation.
Con’t

 Decidual natural killer (NK) cells can regulate trophoblast invasion and vascular growth,
two essential processes in placental development. An abnormal expression of NK cell
surface antigens and a failure in the regulation of NK cell cytotoxicity and cytokines or
angiogenic factors may be some of the causes of pre-eclampsia, resulting in a high-flow
and high-pressure state.
 Consequently, there is a high risk for ischemia-reperfusion injury of the placenta because
of the vasoconstriction of the maternal arteries, which will lead to the formation of
reactive oxygen radicals and further endothelial dysfunction.
Con’t

 The excessive soluble fms-like tyrosine kinase (sFlt)-1 or endoglin and the reduced free
placental growth factor (PlGF) constitute another hypothesis for the pathogenesis of
preeclampsia, namely, the angiogenic imbalance.
 When sFlt-1 levels, which is a variant for PlGF and VEGF, are increased there is an
inactivation or decrease of PlGF and VEGF concentration, resulting in endothelial
dysfunction.
Con’t

 Prostacyclin (PGI2), another potent vasodilator, is decreased in pre-eclamptic women.

This could be due to impaired endothelial Ca2+ signalin, and to the inhibition of PGI2
production by reactive oxygen species (ROS).
 It is still unclear the role of endothelium-derived hyperpolarizing factor (EDHF) in the
vascular pathogenesis of pre-eclampsia, however, EDHF-mediated vasorelaxation is
reduced in vessels from pre-eclamptic pregnancies.
 Pre-eclampsia has also been associated with thrombocytopenia.
Con’t

 Another important feature in pre-eclamptic women is the excessive thrombin generation.

This may be due to different causes (endothelial cell dysfunction, platelet activation,
chemotaxis of monocytes, proliferation of lymphocytes, neutrophil activation, or excessive
generation of tissue factor in response to the activity of proinflammatory cytokines) ending
in the deposition of fibrin in several organ systems.
 Other factors have been implicated in the pathogenesis of pre-eclampsia, including
genetic, environmental, and lifestyle factors.
 On the other hand, excessive weight (body mass index >35 Kg/m2) is an important risk
factor for the disease, with a relative risk of 1.96 in a 95% confidence interval of 1.34–2.87
Figure 2. Proposed mechanism for pre-
eclampsia and eclampsia
Classification

 The American College of

Obstetricians and Gynecologists
(ACOG) in 2000, developed a
classification system for hypertension
during pregnancy, as follows.
Management Preeclampsia with CHF

Obstetric Management
 Obstetric management of pre-eclampsia relies on a high index of suspicion, careful
observation, and early intervention.4 The method of intervention is logically a function of
the severity of the disease, but ultimately the only definitive treatment is delivery of the
fetus and placenta.
Mild pre-eclampsia
 The treatment of mild pre-eclampsia is supportive until delivery and may include complete
or partial bed rest with frequent fetal monitoring as part of expectant management.
Con’t

 Sibai  recommends conservative management of mild pre-eclampsia, since perinatal

outcomes are similar to those in normotensive pregnancies.
 The ACOG practice bulletin on hypertensive disorders unique to pregnancy suggests
monitoring according to the recommendations of the National High Blood Pressure
Education Program Working Group.
 These are fetal monitoring with daily fetal movement counts, weekly nonstress tests or
biophysical profiles, or both, ultrasound examination for fetal growth and amniotic fluid
assessment every 3–4 weeks, maternal tests including BP and laboratory tests to check
hematocrit and platelet count, liver enzymes, renal function, and 12- or 24-hour urine
protein collections at least weekly.
Con’t

Severe pre-eclampsia
 In cases of severe pre-eclampsia, the main goals of therapy are to control BP and to
prevent eclampsia, with vaginal delivery for appropriate patients and cesarean section in
cases of urgency or when induction of labor fails, with timing balanced by the safety of
the mother against the risk of delivery of a potentially premature fetus.
 Expectant management is reserved only for select patients who are far from term but who
are stable on antihypertensive medications, with stable laboratory values and a reassuring
fetal biophysical profile.
 Expectant management should include criteria for delivery and only occur at a tertiary
care hospital with close maternal and fetal monitoring.
Con’t

Anesthetia management
 Management of anesthesia in patients with preeclampsia plays an important role in the
ante partum period. The anesthesiologist must first evaluate pre-anesthesia which includes
the patient's history and physical examination with careful examination of the airway due
to an increased risk of pharyngolaryngeal edema, and an assessment of the patient's
cardiopulmonary condition, fluid, and coagulation status.
 Fasting should be considered in patients who are very active at risk and aim to reduce the
risk of aspiration during cesarean section surgery. Laboratory tests include urine protein,
platelet count, liver enzymes, and coagulation status.
Con’t

 Pulmonary edema is a rare, serious problem complicating as many as 3% of cases of

severe pre-eclampsia.
 An echocardiogram should be obtained if there is any concern of a cardiac etiology (eg,
cardiomyopathy), time permitting. The risk of pulmonary edema increases with age and
parity and often occurs postpartum in association with excess fluid administration or heart
failure.
 In one study of pulmonary edema, maternal mortality was reported to be greater than
10% and perinatal mortality greater than 50%.
Monitoring

 For patients with mild pre-eclampsia, routine monitoring with EKG and automatic blood
pressure cuff is often sufficient. For those with severe preeclampsia, a radial arterial line is
recommended for accurate monitoring of arterial pressures and for sampling of blood for
arterial blood gases, coagulation panel, liver function tests, and serum Mg+ + levels. As
discussed earlier, hemodynamic monitoring should be initiated as needed.
Con’t

 Appropriate understanding of the effects of obstetric interventions that include the use of
magnesium sulfate is important for the management of anesthesia in preeclampsia.

 Magnesium sulfate causes vasodilation directly which can increase uteroplacental blood
flow and lower blood pressure.
Con’t

 For patients with severe pre-eclampsia, it is important to have a flexible anesthetic plan,
preferably with more than one option as the situation may change suddenly without prior
warning. Before any anesthetic intervention, it is important to ensure that hypertension is
well controlled, and concurrent problems, such as eclampsia and pulmonary edema,
treated. Physical examination should include evaluation of the upper airway to document
airway classification.
 Laboratory investigations include complete blood count, coagulation panel, liver function
tests, and urine analysis. Blood and blood products should be ordered as necessary.
Con’t

 The establishment of safe regional anaesthesia (RA) for labour and caesarean delivery in
preeclampsia is one of the most important developments in the past 25 years in obstetric
anaesthesia. Neuraxial anaesthesia offers advantages in preeclampsia in terms of control
of hypertension and simplicity of airway management.
 The indications for general anaesthesia (GA) for caesarean section in preeclamptic
women with preserved ejection fraction are eclampsia with altered mentation
coagulopathy, and thrombocytopaenia.
Con’t

 Several published observational case series describe anaesthesia in eclampsia. Unless the
usual contraindications to regional anaesthesia apply, spinal anaesthesia for caesarean
delivery is the method of choice in patients in whom Glasgow Coma Scale (GCS) is ≥ 14,
antihypertensive and magnesium sulphate therapy has been administered, and cardiac
failure is absent.
 This includes those in whom a difficult tracheal intubation is anticipated. Patients with
persistent decreased level of conciousness who require emergency delivery should
receive a general anaesthetic.
Con’t

 ACOG and the American Society of Anesthesiologists (ASA) recommend regional

anesthesia that is used in patients with preeclampsia without coagulopathy which aims to
reduce the need for general anesthesia which should be done in emergency procedures.
General anesthesia can increase the risk of complications including cerebral hemorrhage
due to changes in blood pressure associated with the effects of rapid induction of
anesthesia.
Con’t

 Regional anesthesia can reduce blood pressure which is usually exacerbated by pain
responses in preeclampsia patients. This usually depends on the patient's hemodynamic
condition and volume status. Giving fluids must always be considered to avoid fluid
overload that can increase the risk of pulmonary edema.

 A number of studies in the past decade have shown that spinal-epidural anesthesia and
combination anesthesia are safe procedures without increasing the risk to the mother and
fetus, even in severe preeclampsia.
Con’t

 Regional anesthesia procedures are often associated with decreased maternal mortality,
but general endotracheal anesthesia (GETA) or general anesthesia is still needed in some
cases. Indications for GETA include suspected placental abortion, coagulopathy, platelet
count less than 80,000 - 10,000 / μL in preeclampsia patients, severe pulmonary edema,
eclampsia, and severe fetal distress.
Con’t

 GETA in preeclampsia can increase the risk of hypertension, aspiration, and transient
neonatal depression; the risk of maternal mortality in GETA ranges from seven times
compared to regional anesthesia. In addition, in preeclampsia patients,
pharyngolaryngeal edema often occurs which of course will be an obstacle in intubation.
Con’t

 Though the severity in presentation of pre-eclampsia varies from different parts of the
world, it remains a major contributor to maternal and fetal morbidity and mortality. The
basis of management remains the same.
 The ominous signs in severe pre-eclampsia are acute respiratory distress syndrome (ARDS),
cerebral edema, intracranial haemorrhage, pulmonary edema and ruptured liver.
 Severe pre-eclampsia is a condition in which the systolic arterial blood pressure is above
160 mmHg, and diastolic blood pressure above 110 mmHg and mean-arterial blood
pressure above 120 mmHg, proteinuria, often accompanied by oliguria, headache,
cerebral disturbances, visual disturbances, epigastric pain, pulmonary edema and HELLPS.
Based on the results of research conducted by Oyebamiji at al. in 2015, the challenge of
researchers in providing safe handling of preeclamptic patients with congestive heart
failure and pulmonary congestion is the appropriate anesthetic choice.
Con’t

 The challenges facing us was how best to deliver this patient safely in a setting with limited
anesthetic options.
 General Anaesthesia in the presence of pulmonary congestions and imminent congestive
cardiac failure will not be the best option for this patient, as it can worsen the maternal
condition. Regional anaesthesia was considered, but regional technique in the presence
of heart failure must avoid marked hemodynamic changes and tachycardia.
Con’t

 Incremental epidural is favored in many standard textbooks, but it is not without its own
drawbacks such as unintentional dural puncture, inadequate analgesia and unexpected
high block.
 Spinal anaesthesia is generally considered superior to epidural anaesthesia for caesarean
section because of more predictable distribution of block as well as a denser block.
However, rapid onset of a spinal and its marked cardiovascular changes made it a
delicate choice for the present case.
Con’t

 David Wilkinson in his studies demonstrated the use of low spinal (single shot) in caesarean
sections  He injected 7.5 mg of hyperbaric bupivacaine at L3/L4, patient remains seated
for 5 minutes. Patient then lies supine with a left lateral tilt and slight head-up tilt. In his
studies the procedures were well tolerated and satisfactory to patient.
 Wilkinson technique was an improvement on the use of modified saddle block for
caesarean section described in the text book of anaesthesia.
 Low dose spinal anaesthesia (Wilkinson’s method) was tried in this patient and was found
safe with satisfactory analgesia. The procedure was well tolerated and acceptable to our
patient. The risk of spinal anaesthesia includes hypotension, hypoventilation, total spinal as
well as failed spinal.
Conclusion

 Preeclampsia is a relatively rare syndrome, occurring in about 5-8% of all pregnancies, and
is the third cause of maternal mortality in the United States. The causes are multifactorial,
and this disease is classified as platelet and endovascular dysfunction with
vasoconstriction, capillary permeation, and decreased intravascular volume which
causes multiorgan hypoperfusion with the potential for end-organ damage including
eclampsia seizures.
Con’t

 Careful initial assessment is carried out for anesthesia procedures in patients with
preeclampsia, especially in severe cases. Regional anesthesia is recommended for
patients with preeclampsia. The ASA guideline recommends that regional anesthesia
should be a preliminary consideration except in severe cases where general anesthesia
must be performed, where there will be an increased risk of general anesthesia.
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Con’t

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